Volume expansion predominantly inhibits proximal reabsorption of NaCl rather than NaHCO3

1983 ◽  
Vol 245 (2) ◽  
pp. F272-F275 ◽  
Author(s):  
M. G. Cogan

The present study quantitated the effect of extracellular volume expansion on absolute proximal bicarbonate, chloride, and water reabsorption in 10 Sprague-Dawley rats. Paired free-flow micropuncture measurements were made in the plasma-replete euvolemic state and following 10% body wt isohydric, colloid-free volume expansion. Single nephron glomerular filtration rate and glomerular ultrafiltrate concentration of bicarbonate and chloride were similar in the two conditions. Volume expansion caused absolute proximal reabsorption of bicarbonate to fall by only 7% (from 987 +/- 39 to 920 +/- 53 pmol/min, P less than 0.05). This decrement in bicarbonate reabsorption was compatible with the known increase in bicarbonate permeability and backleak induced by expansion. In contrast, a marked 26% fall in absolute proximal chloride reabsorption occurred (from 1,601 +/- 147 to 1,180 +/- 149 peq/min, P less than 0.005), attributed to alteration in transcellular rather than passive sodium chloride transport. Thus, the decrease in absolute proximal volume reabsorption (from 19.7 +/- 1.0 to 16.7 +/- 1.2 nl/min, P less than 0.005) induced by volume expansion was predominantly a consequence of inhibition of sodium chloride rather than sodium bicarbonate reabsorption.

1971 ◽  
Vol 40 (6) ◽  
pp. 479-486 ◽  
Author(s):  
J. P. Fillastre ◽  
R. Ardaillou ◽  
R. Isaac

1. Distal blockade by simultaneous administration of ethacrynic acid and chlorothiazide was performed in healthy subjects whose extracellular fluid was expanded by iso-osmotic sodium chloride or bicarbonate. The results obtained were compared with those from non-expanded subjects (Ardaillou & Fillastre, 1969). 2. By this technique urine approximates in composition to proximal tubular fluid and may be used to provide information on its composition. As in other mammals, UNa/PNa and Uosm/Posm were close to 1, whatever the experimental conditions. UCl/PCl was always higher and UHCO3/PHCO3 always less than 1. 3. Extracellular fluid expansion with sodium chloride depresses water and sodium reabsorption as shown by the increase of tubular fluid and the diminution of UInul/PInul and TNa/GFR × PNa where TNa and GFR × PNa are respectively the amounts of sodium reabsorbed and filtered per min. It also decreases bicarbonate proximal Tm. The influence on bicarbonate reabsorption is more marked in alkali-loaded than in acid-loaded subjects. 4. Extracellular fluid expansion with iso-osmotic sodium bicarbonate also depresses water, sodium and bicarbonate reabsorption. These results suggest that chloride administration is not necessary to diminish bicarbonate reabsorption and that tubular reabsorption of bicarbonate depends in part on the state of effective extracellular volume.


1990 ◽  
Vol 259 (4) ◽  
pp. F565-F572 ◽  
Author(s):  
J. Schnermann ◽  
J. P. Briggs

Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.


PEDIATRICS ◽  
1976 ◽  
Vol 58 (3) ◽  
pp. 370-377
Author(s):  
Billy S. Arant ◽  
Ira Greifer ◽  
Chester M. Edelmann ◽  
Adrian Spitzer

A male child discovered to have cystinosis and Fanconi syndrome at the age of 2 years 8 months was hospitalized repeatedly for episodes of hyponatremic, hypokalemic dehydration and acidosis. Attempts to correct the fluid and electrolyte abnormalities by increasing progressively the supplements of sodium chloride, sodium bicarbonate, and potassium chloride resulted only in an exacerbation of the symptoms. Tests of discrete renal functions and metabolic balance studies disclosed that, although all disturbances were expressions of the primary disease, their severity was enhanced considerably by the extracellular volume expansion induced by the vigorous therapy. Restriction in water intake resulted in an improvement in the renal performance and in the clinical condition.


1978 ◽  
Vol 54 (3) ◽  
pp. 333-336
Author(s):  
N. Ish-Shalom ◽  
J. Rapoport ◽  
C. Chaimovitz ◽  
O. S. Better

1. The effect of extracellular volume expansion (ECVE) during water diuresis, and of water diuresis alone, on the formation of free water in man was compared. 2. ECVE reduced free water formation at any given rate of distal delivery compared with water diuresis. Thus, ECVE depresses distal sodium chloride reabsorption. 3. This attenuation of free water formation occurred both when urine flow (V/100 ml glomerular filtration rate) and distal chloride delivery [(Cwater + CCl)/100 ml glomerular filtration rate] were used as the terms for distal delivery. 4. We suggest that the distal depression of sodium chloride reabsorption after ECVE is probably due to a direct inhibition of distal sodium chloride transport mechanisms, and not to the flooding of the diluting site by the poorly reabsorbable bicarbonate ion.


1969 ◽  
Vol 130 (4) ◽  
pp. 1276-1279 ◽  
Author(s):  
S. G. Massry ◽  
H. Vorherr ◽  
C. R. Kleeman

2008 ◽  
Vol 28 (4) ◽  
pp. 407-412 ◽  
Author(s):  
M.-José Fernández-Reyes ◽  
M.-Auxiliadora Bajo ◽  
Gloria del Peso ◽  
Dabaiba Regidor ◽  
Covadonga Hevia ◽  
...  

1994 ◽  
Vol 267 (1) ◽  
pp. F99-F105 ◽  
Author(s):  
K. Ohishi ◽  
M. I. Okwueze ◽  
R. C. Vari ◽  
P. K. Carmines

This study was designed to identify and localize defects in renal microvascular function during the hyperfiltration stage of diabetes mellitus. Male Sprague-Dawley rats were injected intravenously with 65 mg/kg streptozotocin (IDDM rats) or vehicle (sham rats). IDDM rats received insulin (3 U.kg-1.day-1) via an osmotic minipump; sham rats received diluent. During the ensuing 2-wk period, blood glucose levels averaged 89 +/- 2 mg/dl in 33 sham rats and 290 +/- 13 mg/dl in 37 IDDM rats. At the end of this period, inulin clearance was elevated in eight IDDM rats (1.43 +/- 0.17 ml.min-1.g kidney wt-1) compared with six sham rats (0.78 +/- 0.05 ml.min-1.g kidney wt-1). The remaining animals served as tissue donors for study of the renal microvasculature using the in vitro blood-perfused juxtamedullary nephron technique. Kidneys from sham and IDDM rats were perfused with homologous blood at a renal arterial pressure of 110 mmHg. Juxtamedullary single-nephron glomerular filtration rate was higher in IDDM rats (41.5 +/- 5.4 nl/min) than in sham rats (25.4 +/- 2.4 nl/min). Afferent arteriolar inside diameter was greater in IDDM rats (34 +/- 2 microns) than in sham rats (22 +/- 1 microns); however, efferent arteriolar diameter did not differ between groups. The afferent arteriolar vasoconstrictor response to norepinephrine (NE) was attenuated in IDDM rats, relative to sham rats, over a wide range of NE concentrations. In contrast, NE evoked similar degrees of efferent vasoconstriction in IDDM and sham rats.(ABSTRACT TRUNCATED AT 250 WORDS)


Sign in / Sign up

Export Citation Format

Share Document